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WAS, WASP actin nucleation promoting factor

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WAS, WASP actin nucleation promoting factor

  • The Wiskott-Aldrich syndrome (WAS) family of proteins share similar domain structure, and are involved in transduction of signals from receptors on the cell surface to the actin cytoskeleton. The presence of a number of different motifs suggests that they are regulated by a number of different stimuli, and interact with multiple proteins. Recent studies have demonstrated that these proteins, directly or indirectly, associate with the small GTPase, Cdc42, known to regulate formation of actin filaments, and the cytoskeletal organizing complex, Arp2/3. Wiskott-Aldrich syndrome is a rare, inherited, X-linked, recessive disease characterized by immune dysregulation and microthrombocytopenia, and is caused by mutations in the WAS gene. The WAS gene product is a cytoplasmic protein, expressed exclusively in hematopoietic cells, which show signalling and cytoskeletal abnormalities in WAS patients. A transcript variant arising as a result of alternative promoter usage, and containing a different 5' UTR sequence, has been described, however, its full-length nature is not known. [provided by RefSeq, Jul 2008]

  • Gene Synonyms (wiskott-Aldrich syndrome protein, eczema-thrombocytopenia, thrombocytopenia 1 (X-linked), IMD2, SCNX, THC, THC1, WASP, WASPA,)
  • NCBI Gene ID: 7454
  • Species: Homo sapiens (Human)
  • UNIPROT ID#>>P42768
    UNIPROT ID#>>A0A024QYX8
  • View the NCBI Database for this Gene »

The information on this page was collected from publicly accessible databases, and is periodically updated. Promega makes no claims to accuracy, or ownership of these genes.

Gene products are often involved in multiple pathways and networks within a living cell. Learn more about other interacting partners.

WASP actin nucleation promoting factor interacts with:

The information on this page was collected from publicly accessible databases, and is periodically updated. Promega makes no claims to accuracy, or ownership of these genes.

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The information on this page was collected from publicly accessible databases, and is periodically updated. Promega makes no claims to accuracy, or ownership of these genes.

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